Osteoarthritis develops in the operated joint of an ovine model following ACL reconstruction with immediate anatomic reattachment of the native ACL

We tested the hypothesis that immediate reattachment of the native anterior cruciate ligament (ACL) can prevent kinematic changes and the development of osteoarthritis (OA). Five sheep underwent anatomic unilateral ACL reconstruction (ACL‐R). Animals from a previous study served as sham (n = 7) or non‐operated (n = 17) controls. At 4 points of walking gait, 6 degrees of freedom stifle joint kinematics of ACL‐R animals were compared with sham controls at 4 and 20 weeks post‐surgery. Gross cartilage, bone, and meniscal changes were graded at euthanasia; paired and differential scores were compared. Inter‐animal differences were noted in all groups. Of 48 points of gait comparison between ACL‐R and sham operated groups, 42 points showed no difference (p > 0.05). Of the six significant differences (p < 0.05), internal rotation in ACL‐R animals accounted for three. At 20 weeks, differential scores showed that sham operated joints were morphologically indistinguishable from non‐operated controls (p ≥ 0.129) while ACL‐R joints had significantly higher combined cartilage and osteophyte scores than those controls (p ≤ 0.003). This method of ACL reconstruction in sheep did not restore normal walking gait kinematics completely and allowed some OA to develop in operated joints. OA may result from relatively subtle mechanical abnormalities, apparently more so in some individuals than others. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 31:35–43, 2012     

Periarticular ligament changes following ACL/MCL transection in an ovine stifle joint model of osteoarthritis.

Anterior cruciate ligament (ACL) injuries often lead to significant functional impairment, and are associated with increased risk for induction of degenerative joint disease. However, few studies have described the effect of ligament transection on the remaining intact knee ligaments. This study sought to determine specifically what impact combined ACL/medial collateral ligament (MCL) transection had on the remaining intact knee ligaments, particularly from the histological, biochemical, and molecular perspectives. Twenty weeks post-ACL/MCL transection, the cut ends of sheep MCLs were bridged by scar, while the posterior cruciate ligaments (PCLs) and lateral collateral ligaments (LCLs) seemed gross morphologically normal. Water content and cell density increased significantly in the MCL scars and the intact PCLs but were unchanged in the LCLs. Collagen fibril diameter distribution was significantly altered in both MCL scar tissue and uninjured PCLs from transected joints. MMP-13 mRNA levels in MCL scars and PCLs from ligament transected joints were increased, while TIMP-1 mRNA levels were significantly decreased in the PCLs only. This study has shown that some intact ligaments in injured joints are impacted by the injury. The joint appears to behave like an integrated organ system, with injury to one component affecting the other components as the "organ" attempts to adapt to the loss of integrity.     

Vascular adaptation of intact joint stabilizing structures in the posterior cruciate ligament deficient rabbit knee.

Loss of the posterior cruciate ligament (PCL) of the knee has a significant impact on joint stability and biomechanical function. Changes in joint biomechanics may result in mal-adaptive tissue degeneration and functional alteration of supporting ligaments. This study examines the effects of joint laxity on the vascular physiology of the intact anterior cruciate (ACL) and medial collateral (MCL) ligaments after PCL transection in rabbits.One-year-old female New Zealand white rabbits were assigned to control (n=12), sham-operated (n=12) or PCL transected (2, 6 or 16 weeks, n=12 per time point) groups. Half of the animals (n=6 per group) were used for ACL and MCL blood flow determination using coloured microsphere infusion (ml/min/100 g), and half were used for vascular volume determination (given as vascular index, micro l/g).In the MCL, PCL transection induced large, significant (4-5-fold) increases in blood flow (peak at 2 weeks) and vascular index (peak at 6 weeks) compared to sham-operated animals that returned towards control values by 16 weeks. In contrast, the ACL showed no increase in blood flow in lax joints, and a relatively small (2-fold) increase in vascular index at 6 weeks only. The wet weight and water content of both the MCL and ACL were significantly increased in PCL-deficient joints.We conclude that joint laxity (instability) subsequent to loss of the PCL in rabbits impacts the vascular physiology of intact supporting ligaments, inducing both vasomotor and angiogenic responses in the MCL. Changes in wet weight and water content of both the MCL and ACL demonstrate prolonged physiological adaptation of intact structures in lax joints.     

The early effects of joint immobilization on medial collateral ligament healing in an ACL-deficient knee: a gross anatomic and biomechanical investigation in the adult rabbit model.

In this study, the short-term effects of immobilization on joint damage and medial collateral ligament (MCL) healing were investigated in unstable, anterior cruciate ligament (ACL)-deficient knees in rabbits. Forty-six 12-month-old female New Zealand white rabbits were separated into three groups. Animals from each group had surgery on their right knees: group I, sham controls (n = 9); group II, complete transection of the ACL and removal of a 4 mm segment (gap injury) of MCL midsubstance with no immobilization of the limb (n = 19); and group III, same injuries to the ACL and MCL (as group II) but with immobilization of the limb (n = 18). No surgical repair of disrupted ligaments was performed. Left knees served as unoperated contralateral controls. All animals were allowed unrestricted cage activity until sacrifice in subgroups at 3, 6, and 14 weeks of healing when biomechanical properties of all MCLs were measured. All knee joints were systematically examined for gross evidence of damage to articular cartilage, menisci, and periarticular soft tissues. To monitor relative in vivo loads on injured limbs during healing, hindlimb weight bearing was assessed at biweekly intervals. Results indicated that animals in both groups II and III bore relatively lower loads (compared to preinjury values) on their injured hindlimbs. Mechanical testing of MCLs showed only minor changes in sham controls, while group II and III healing MCLs demonstrated significantly lower force and stress at MCL complex failure compared to contralateral controls. In specific comparisons of group III to group II animals, we noted that immobilization prevented joint damage over the early intervals studied. In addition, immobilization resulted in MCL laxity similar to contralateral control values but inhibited development of structural strength and stiffness in healing MCLs. These results suggest that in the rabbit, short-term immobilization of an ACL-deficient knee offers some advantages to the joint and to certain low load behaviors of the healing MCL, but it also results in a smaller quantity of scar tissue that is less able to resist higher loads. Longer-term studies involving remobilization are necessary before the effects of brief immobilization on joint damage and MCL healing in this ACL-deficient model can be fully defined.     

ACL transection influences mRNA levels for collagen type I and TNF-alpha in MCL scar.

To assess the mRNA expression of extracellular matrix genes which might correlate with or contribute to mechanically weaker medial collateral ligament (MCL) scars in the ACL-deficient rabbit knee joint compared to those in anterior cruciate ligament (ACL) intact knee joints, a bilateral MCL injury was induced in 10 skeletally mature female NZW rabbits. As part of the same surgical procedure, the ACL was transected in one of the knees while the contralateral knee had a sham procedure. The side having the combined MCL and ACL injury was randomly assigned. After six weeks, the rabbits were euthanized. Histological assessments were performed on samples of the MCL scars from each operated knee (n = 3 animals) and mRNA levels for collagen type I, III, V, decorin, biglycan, lumican, fibromodulin, TGF-beta, IL-1, TNF-alpha, MMP-1, MMP-13, and a housekeeping gene (GAPDH) were assessed using semiquantitative RT-PCR on RNA isolated from the MCL scar tissue of the remaining animals (n = 7 animals). Levels of mRNA for each gene were normalized using the corresponding GAPDH value. Results showed that the total RNA yield (per mg wet weight) in the MCL scar of the ACL-deficient knee was significantly greater than that in the MCL scar from the ACL-intact knee. Collagen type I mRNA levels were significantly lower and mRNA levels for TNF-alpha were significantly greater in the scars of ACL-deficient knees compared to scars from ACL-intact joints. There were no significant differences between ACL-deficient and ACL-intact knees with respect to MCL scar mRNA levels for the remaining genes assessed. Histologically, the "flaw" area, which has been shown to correlate with mechanical properties in previous studies, was significantly greater in MCL scars from ACL-deficient knees than in the ACL-intact MCL scars. The mean number of cells/mm2 in MCL scars from ACL-deficient knees was significantly greater than in MCL scars from ACL-intact knees. The present study suggests that MCL scar cell metabolism is differentially influenced by the combined injury environment.     

Antiresorptive therapy conserves some periarticular bone and ligament mechanical properties after anterior cruciate ligament disruption in the rabbit knee

The purpose of this study was to assess, in an osteoarthritic (OA) model, whether bisphosphonate (BP) antiresorptive therapy altered periarticular bone and bone–ligament biomechanics and OA progression. We surgically transected the anterior cruciate ligament (ACLX) in two groups of rabbits; the first group was dosed with BP (risedronate, 0.01 mg/kg s.c. daily for 6 wk), the second group remained untreated, and a third group of normal (unoperated) control rabbits was also evaluated. We measured distal femoral bone mineral density (BMD, Dual Energy X‐ray Absorptiometry [DEXA]), medial collateral ligament (MCL) laxity, and bone mechanical function (bone cores mechanically tested in compression). These measures were related to cartilage/joint gross morphology, histology, and measures of vascular volume (gelatin–dye perfusion) for evidence of inflammatory angiogenesis and early OA. BMD by DEXA in 6 wk ACLX animals was 18% less than normal controls (p < 0.05). In contrast, BP dosing conserved periarticular BMD; risedronate‐treated rabbits had distal femoral BMD only 5% less and not significantly different than normal controls. When the same bone cores were compressed to failure, both ACLX and BP‐dosed animals were significantly weaker than normal controls (p < 0.05). However, the bone energy to failure and elastic modulus of BP‐dosed animals was conserved and not significantly different from normal controls 6 wk after ACLX. Blocking bone resorption with BP also resulted in a significantly improved bone–ligament structural complex. MCL‐complex laxity was significantly less in BP‐dosed animals (1.2 times that of normal controls) compared to untreated ACLX animals (1.7 times that of normal controls; p < 0.05). Blocking bone resorption with risedronate did not suppress osteophytosis and inflammatory angiogenesis, which were significantly increased in the periarticular bone of both untreated and BP treated ACLX animals. Thus, administering BP immediately after ACL loss conserved some periarticular bone and MCL‐complex properties in an early OA model. © 2004 Published by Elsevier Ltd. on behalf of Orthopaedic Research Society.     

Correlation of healing capacity with vascular response in the anterior cruciate and medial collateral ligaments of the rabbit.

In clinical terms, functional recovery after anterior cruciate ligament (ACL) injury is generally poorer than after medial collateral ligament (MCL) injury. In experimental studies of injury, the early phases of ligament healing require an augmented blood supply. We hypothesized that the differences in healing properties of the ACL and MCL would be reflected in the magnitude of their vascular responses to partial injury. This study is the first to quantify and define the time course of changes in blood flow and vascular volume following hemisection of the rabbit ACL and MCL.Adult female rabbits were assigned to control, sham operation, ACL hemisection or MCL hemisection groups. Standardized ACL or MCL injuries were surgically induced. About 2, 6 or 16 weeks later, blood flow and vascular volume of the ACL and MCL were measured.The MCL of the rabbit responded to hemisection with a large significant increase in blood flow and a substantial angiogenic response associated with inflammation and scar formation. During subsequent matrix remodelling, blood flow and vascular volume returned towards control values. In contrast, the ACL showed only a 2-fold increase in vascular volume, no increase in blood flow and atrophied after hemisection. The superior capacity of the MCL to increase its blood supply through angiogenesis and increased flow is essential for ligament healing to occur, and may be the major difference in healing potential between the ACL and MCL.     

Posttraumatic incarceration of medial collateral ligament into knee joint with anterior cruciate ligament injury

Medial collateral ligament of the knee is an important coronal stabiliser and often injured in isolation or as combination of injuries. The article reports a case of incarcerated medial collateral ligament (MCL) injury in combination with anterior cruciate ligament (ACL) injury in 20 year old male who presented to us 4 weeks after injury. Clinical examination and MRI was correlated to complete ACL tear with torn distal MCL and incarceration into the joint. Patient was taken up for ACL hamstring graft reconstruction with mini-arthrotomy and repair of the torn MCL. Patient was followed up with dedicated rehabilitation protocol with good functional results. At one year follow-up, patient exhibited full range of motion with negative Lachman, Pivot shift and valgus stress tests. This article highlights the rare pattern of MCL tear and also reviews the literature on this pattern of injury.     

Healing of the medial collateral ligament following a triad injury: a biomechanical and histological study of the knee in rabbits.

The effect of a partial medial meniscectomy and anterior cruciate ligament (ACL) transection on medial collateral ligament (MCL) healing was studied in skeletally mature rabbits. Two groups of animals, group I (isolated MCL rupture) and group II (MCL rupture with ACL transection and partial medial meniscectomy), were examined. At 6 and 12 weeks postoperatively, histological examination of the healing MCL and biomechanical evaluation of the varus-valgus (V-V) knee rotation and tensile properties of the femur-MCL-tibia complex (FMTC) were performed. Group II animals experienced substantial joint degeneration by 6 weeks. Progressive osteophyte formation was observed adjacent to the MCL insertions along with proximal migration of the MCL tibial insertion between 6 and 12 weeks. Histologic examination of the healing MCL substance from both groups showed disorganized collagen, inflammation, and fibroblast proliferation that decreased over time. For group II knees, the V-V knee rotation was found to be significantly elevated (4.7 to 5.2 times the contralateral control), and did not decrease with time. In contrast, the V-V knee rotations of the group I specimens were 1.8 times greater than control immediately following injury, and approached control values by 12 weeks. Tensile testing of the FMTCs revealed that the ultimate load increased with time for both groups, but group I had significantly higher values than group II. The linear stiffness in group I was not different than that group II and did not increase with time. For the mechanical (material) properties of the healed MCL substance, the modulus of the healing tissue for group II was only 40% that of group I. The structural properties of the FMTC and the mechanical properties of the MCL substance from both groups at 6 and 12 weeks were significantly different from the contralateral controls. We further demonstrated that immediately after ACL reconstruction, the V-V rotation of group II knees could be restored to group I levels. Recent clinical studies of MCL healing following isolated complete ligament tears have suggested that nonoperative management without immobilization leads to excellent treatment outcome. However, in more severe injuries involving additional tissues, poor quality of the healed ligament tissue and articular degeneration are observed. Our results demonstrate the deleterious effects of an untreated triad injury on the healing of the MCL substance and its insertions. Examination of the MCL substance suggests that a much larger healing mass is formed following a triad injury, which partially compensates for inferior ligament mechanical properties.(ABSTRACT TRUNCATED AT 400 WORDS)     

分期修复重建膝关节多发韧带损伤的临床疗效

目的 :探讨关节镜下分期治疗膝关节多发韧带损伤的临床疗效。方法 :2006年3月至2012年6月,关节镜下分期治疗膝关节多发韧带损伤14例(14膝)。男8例,女6例;年龄20~49岁,平均(31.8±8.1)岁。患者均行X线、MR检查,提示10例前交叉韧带、后交叉韧带及内侧副韧带损伤,4例前交叉韧带、后交叉韧带及后外侧角损伤。合并内侧半月板损伤4例,外侧半月板损伤2例。Ⅰ期手术治疗内侧副韧带损伤、后交叉韧带及半月板,术后固定3周后开始主被动功能锻炼,3~6个月后膝关节活动范围正常且存在明显松弛时Ⅱ期重建前交叉韧带和(或)后交叉韧带。结果:术后切口均Ⅰ期愈合,无感染等手术相关并发症发生。患者均获随访,时间24~80个月,平均48.9个月。末次随访时膝关节Lysholm评分达87.1±2.8,优于术前19.6±0.9(t=12.3,P0.01)。国际膝关节评分委员会(International Knee Documentation Committee,IKDC)评级:9例接近正常,5例异常。结论 :关节镜下分期治疗膝关节多发韧带损伤能有效恢复膝关节稳定性和功能。     

Vascular structure and function in the medial collateral ligament of anterior cruciate ligament transected rabbit knees

To determine if decreased vascular responsiveness in the medial collateral ligament (MCL) of anterior cruciate ligament transected (ACL‐t) rabbit knees is due to pericyte deficiency associated with angiogenesis. Vascular responses to potassium chloride (KCl), phenylephrine, acetylcholine, and sodium nitroprusside (SNP) were evaluated in ACL‐t rabbit knees (n = 6) and control knees (n = 5) using laser speckle perfusion imaging. Ligament degeneration was determined by ultrasound imaging. Vascular and pericyte volume were measured using quantitative immunohistochemical volumetric analysis using CD31 and α‐smooth muscle actin antibodies with co‐localization analysis. Perfusion was increased in the ACL‐t rabbits 2.5‐fold. Responsiveness to phenylephrine, SNP, and acetylcholine was significantly decreased in the ACL knee while no change in KCl responses was seen. MCL ultrasound imaging revealed decreased collagen organization, increased ligament thickness, and increased water content in the ACL‐t MCL. Vascular Volume was increased fourfold in ACL deficient knees, while pericyte volume to endothelial volume was not changed. No difference in CD31 and α‐SMA co‐localization was found. Blood vessels in the MCL of ACL‐t knees do not lack smooth muscle. The MCL vasculature can undergo constrictive response to KCl, but have impaired receptor mediated responses and impaired nitric oxide signaling. © 2014 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 32:1104–1110, 2014.     

Neural stimulation does not mediate attenuated vascular response in ACL‐deficient knees: Potential role of local inflammatory mediators

Chronic inflammation associated with osteoarthritis (OA) alters normal responses and modifies the functionality of the articular vasculature. Altered responsiveness of the vasculature may be due to excessive neural activity associated with chronic pain and inflammation, or from the production of inflammatory mediators which induce vasodilation. Using laser speckle perfusion imaging (LSPI), blood flow to the medial collateral ligament (MCL) of adult rabbits was measured in denervated ACL transected knees (n = 6) and compared to unoperated control (n = 6) and 6‐week anterial cruciate ligament (ACL)‐transected knees (n = 6). Phenylephrine and neuropeptide Y were applied to the MCL vasculature in topical boluses of 100 µL (dose range 10^?14 to 10^?8 mol and 10^?14 to 10^?9 mol, respectively). Denervation diminished vasoconstrictive responsiveness to phenylephrine compared to both control and ACL‐transected knees. Denervation minimally enhanced vascular responses to neuropeptide Y (NPY) compared to ACL deficiency alone, which nevertheless remained significantly diminished from control responses. To evaluate the potential role of inflammatory dilators in the diminished contractile responses, phenylephrine was coadministered with histamine, substance P, and prostaglandin E₂. High‐dose histamine, and low‐dose substance P and PGE₂ were able to inhibit contractile responses in the MCL of control knees. Excessive neural input does not mediate diminished vasoconstrictive responses in the ACL transected knee; inflammatory mediators may play a role in the deficient vascular responsiveness of the ACL transected knee. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 28:83–88, 2010     

Decreased posterior cruciate and altered collateral ligament loading following ACL transection: A longitudinal study in the ovine model

Although ACL deficiency is shown to lead to joint degeneration, few quantitative data are reported on its effect on soft tissue structures surrounding the knee joint, specifically, the posterior cruciate and collateral ligaments. The kinematics of the stifle joint of sheep (N = 5) were measured during “normal” gait, as well as 4 and 20 weeks after ACL transection. These motions were reproduced using a unique robotic manipulator and the loads borne by PCL, MCL, and LCL during gait were determined. Our results demonstrated a significant decrease in mean PCL loads 20 weeks post‐ACL injury, at hoof‐strike (0% of gait, p = 0.034), hoof‐off (66% of gait, p = 0.006), peak‐swing (85% of gait, p = 0.026), and extension‐before‐hoof‐strike (95% of gait, p = 0.028). Mean MCL loads did not significantly increase following ACL transection, maybe due to large between‐animal variation. Finally, mean LCL loads indicated a significant decrease (p < 0.047) at 20 weeks across the entire gait cycle. From a clinical perspective, the load redistributions observed in cruciate and collateral ligaments following ACL injury indicate that these tissues can carry/adapt to the altered mechanical environment of the joint. The considerable variability in the magnitudes of change following ACL injury among animals also simulates clinical variability in humans after trauma. © 2013 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 32:431–438, 2014.     

Immediate ACL reconstruction prevents microvascular pathophysiology in the Uninjured MCL that is not fully reversed by delayed ACL reconstruction

Anterior cruciate ligament (ACL) injury induces maladaptive vascular responses that degrade medial collateral ligament (MCL) function. The purpose of this study was to determine if early or delayed ACL reconstruction can prevent or reverse the abnormal changes in vascular function that occur in the uninjured MCL after ACL injury. Twenty‐four rabbits were divided into four groups (n = 6); control, ACL‐deficient (ACL‐X), immediate ACL reconstructed (ACL‐IR) and delayed ACL reconstructed (ACL‐DR). After 8 weeks, MCLs were assessed for blood flow, responses to acetylcholine (ACh) and phenylephrine (Phe) and autoregulatory responses, using laser speckle perfusion imaging. In ACL‐X knees, blood flow in the MCL increased by 2.5‐fold compared to control. MCL hyperemia was diminished in ACL‐DR knees and was unaltered in ACL‐IR knees. MCL vasculature was unresponsive to ACh and Phe in ACL‐X. These responses were partially restored by ACL reconstruction. Autoregulatory responses were not significantly different between groups. ACL‐DR decreased hyperemia in the MCL and partially attenuated abnormal MCL vascular responses. ACL‐IR was more effective at preventing MCL hyperemia and preserving vascular responsiveness to ACh and Phe. This suggests that the vascular alterations in the uninjured rabbit MCL are largely caused by abnormal mechanical loading resulting from ACL deficiency and can be prevented through early reconstruction. Early ACL reconstruction could limit the progression of microvascular dysfunction of the MCL, and preserve physiological joint homeostasis. This might prevent joint degeneration and delay the progression of osteoarthritis. © 2011 Orthopaedic Research Society Published by Wiley Periodicals, Inc. J Orthop Res 29: 1390–1396, 2011     

Comparison between two rabbit models of posttraumatic osteoarthritis: A longitudinal tear in the medial meniscus and anterior cruciate ligament transection

Animal osteoarthritis (OA) models have been developed to understand OA progression and evaluate new OA therapies. However, individual variations in joint lesions remain a critical problem in most current OA models. We established a novel rabbit model by creating a longitudinal tear in the medial meniscus body that was reproducible and similar to posttraumatic biomechanical disturbances in human OA. New Zealand rabbits underwent surgery and were assessed for 9 weeks. The rabbits were randomized into the sham control, medial meniscal tear (MMT), and anterior cruciate ligament transection (ACLT) groups. The animals were sacrificed at 4, 6, and 9 weeks posttreatment. The knee joints were harvested for histological and gene expression assessments. Both the MMT and ACLT procedures led to time-dependent degenerative changes in the femoral condyle cartilage. At each time point, the MMT group cartilage showed more severe degenerative changes than did the ACLT group cartilage. Consistently, inflammatory cytokine and catabolic gene expression were significantly higher, and anabolic gene expression was significantly lower in the MMT group than in the ACLT group. MMT treatment caused more severe structural damage to the cartilage and higher catabolic gene expression levels than the ACLT model at each time point. The MMT model may be highly beneficial in investigating posttraumatic OA (PTOA) development, especially PTOA from a meniscal injury. The MMT model replicated key features of human PTOA, including meniscal lesions, inflammatory responses, and the progression to osteoarthritic cartilage degeneration, thereby providing an exciting new avenue for translating promising treatments to clinical practice.     

Factors for the presence of anteromedial rotatory instability of the knee

Anteromedial rotatory instability (AMRI) of the knee joint was investigated with an instrument newly designed to simulate the manual AMRI test and to quantify its magnitude. Thirty healthy subjects, 20 patients with anterior cruciate ligament (ACL) injury, and 10 with both ACL and medial collateral ligament (MCL) injuries were examined. Using the instrument, 100N of anterior force was applied to the proximal part of the tibia with the foot in neutral rotation, 30° of internal rotation, and 30° of external rotation, and the magnitude of anterior displacement was recorded. The measurement was carried out at 20° and 90° of flexion. A significant increase in anterior laxity was observed in all three rotation positions in the injured patients. However, the magnitude of laxity in external rotation was less than that in neutral rotation in the ACL injured patients, whereas it was the greatest in external rotation in ACL + MCL injured patients. Thus, we conclude that an injury involving both the ACL and MCL causes AMRI.     

Biological and Biomechanical Evaluation of Autologous Tendon Combined with Ligament Advanced Reinforcement System Artificial Ligament in a Rabbit Model of Anterior Cruciate Ligament Reconstruction

Objective

To compare the biomechanical and histological changes in a rabbit model after reconstructing the anterior cruciate ligament (ACL) with solely autologous tendon and with autologous tendon combined with the ligament advanced reinforcement system (LARS) artificial ligament.

Methods

Anterior cruciate ligament reconstruction was performed in 72 knees from 36 healthy New Zealand white rabbits (bodyweight, 2500–3000 g). The Achilles tendons were harvested bilaterally. The left ACL were reconstructed solely with autografts (autologous tendon group), while the right ACL were reconstructed with autografts combined with LARS ligaments (combined ligaments group). The gross observation, histological determination, and the tension failure loads in both groups were evaluated at 12 weeks (n = 18) and 24 weeks (n = 18) postoperatively.

Results

Gross examination of the knee joints showed that all combined ligaments were obviously covered by a connective tissue layer at 12 weeks, and were completely covered at 24 weeks. Fibrous tissue ingrowth was observed between fascicles and individual fibers in the bone–artificial ligament interface at both time points; this fibrovascular tissue layer localized at the bone–artificial ligament interface tended to be denser in specimens obtained at 24 weeks compared with those obtained at 12 weeks. The tension failure loads of the knees were similar in the autologous tendon group and the combined ligaments group at 12 weeks (144.15 ± 3.92 N vs. 140.88 ± 2.75 N; P > 0.05), and at 24 weeks (184.15 ± 1.96 N vs. 180.88 ± 3.21 N; P > 0.05).

Conclusion

Reconstructing the ACL in rabbits using autologous tendon combined with the LARS artificial ligament results in satisfactory biointegration, with no obvious immunological rejection between the autologous tendon and the artificial ligament, and is, therefore, a promising ACL reconstruction method.

     

A comparison of joint stability between anterior cruciate intact and deficient knees: a new canine model of anterior cruciate ligament disruption.

Transection of the canine anterior cruciate ligament (ACL) is a well-established osteoarthritis (OA) model. This study evaluated a new method of canine ACL disruption as well as canine knee joint laxity and joint capsule (JC) contribution to joint stability at two time points (16 and 26 weeks) after ACL disruption (n=5/time interval). Ten crossbreed hounds were evaluated with force plate gait analysis and radiographs at intervals up to 34 weeks after monopolar radiofrequency energy (MRFE) treatment of one randomly selected ACL. Each contralateral ACL was sham treated. The MRFE treated ACLs ruptured approximately eight weeks (mean 52.5 days, SEM+/-1.0, range 48-56 days) after treatment. Gait analysis and radiographic changes were consistent with established canine ACL transection models of OA. Anterior-posterior (AP) translation and medial-lateral (ML) rotation were measured in each knee at 30 degrees, 60 degrees, and 90 degrees of flexion with and then without JC with loads of 40 N in AP translation and 4 Nm in ML rotation. A statistically significant interaction in AP translation included JC by cruciate (P=0.02), and there was a trend for a cruciate by time (P=0.07) interaction. Significant interactions in ML rotational testing included the presence of joint capsule (P=0.0001) and angle by cruciate (P=0.0012). This study describes a model in which canine ACLs predictably rupture approximately eight weeks after arthroscopic surgery and details the contribution of JC to canine knee stability in both ACL intact and deficient knees. The model presented here avoids the introduction of potential surgical variables at the time of ACL rupture and may contribute to studies of OA pathogenesis and inhibition. This model may also be useful for insight into the pathologic changes that occur in the knee as the ACL undergoes degeneration prior to rupture.     

Evaluation of the muscles around the knee in rabbits whose anterior cruciate and/or medial collateral ligaments were dissected

Introduction The biological response of the muscles around the knee in chronic ligamentous instability was investigated in an animal study.Materials and methods There were four groups of 6- to 9-month-old adult New Zealand albino rabbits (2500–3300 g). The animals were divided into groups according to the ligament that was surgically sectioned: group A anterior cruciate ligament (ACL), group B medial collateral ligament (MCL), group C both ACL and MCL, and group D served as the control group undergoing no surgical intervention. Three months after surgery, biopsy specimens of the vastus lateralis, rectus femoris, biceps femoris, extensor digitorum longus, and gastrocnemius muscles of the rabbits were obtained. Electron-microscopic cross-sections of the biopsy specimens were evaluated using the new predetermined atrophy parameters.Results Atrophy was found in the biopsy specimens of the quadriceps muscles in groups A and C (p<0.005). Unimportant changes were seen in the hamstrings, extensor digitorum longus, and gastrocnemius muscles (p>0.05). Only in the group undergoing MCL dissection were no changes observed in the muscles (p>0.05).Conclusion It is concluded that ACL lesions affect the biomechanics of the knee negatively and this situation causes atrophy, especially in the quadriceps muscle. An MCL lesion alone does not cause an important problem in the surrounding musculature, probably because of its spontaneous healing capacity. New criteria for assessment of atrophy in the muscles employing electron-microscopic evaluation are suggested.     

Vascular physiology and long-term healing of partial ligament tears.

Functional outcomes of anterior cruciate ligament (ACL) injury are generally poorer than those of medial collateral ligament (MCL) tears. Following ligament damage, all phases of ligament healing require an adequate blood supply. We hypothesized that the differences in healing properties of the ACL and MCL would reflect their vascular responses to joint injury. This paper examines the long-term changes in blood flow and vascular volume of rabbit knee ligaments after direct injury, and under conditions of chronic joint instability induced by section of the posterior cruciate ligament (PCL). Standardized injuries were surgically induced in adult rabbit knee ligaments: partial MCL transection, partial ACL transection, or complete PCL transection (joint instability). Sixteen weeks later the blood flow and vascular volume of the ACL and MCL were measured and compared to control and sham-operated animals. Direct ligament injury induced significant increases in standardized blood flow and vascular volume of both ACL and MCL after 16 weeks; however, the vascular volume of the ACL was not higher than the control levels in the MCL. We conclude that direct injury to both the anterior cruciate and MCLs induces long-term physiological responses. Joint laxity is a common sequel to PCL injury. Chronic joint laxity failed to induce adaptive vascular responses in the ACL, while the MCL shows significant amplification of blood supply. Although both MCL and ACL showed increased weight after PCL transection, the lack of a long-term vascular response in the ACL may be a major factor in its the diminished healing potential.